1) Two recording electrodes (G1 and G2) are placed over the nerve, 3.5 to 4 cm apart

2) G1, the active recording electrode, is placed closer to stimulator

3) Ground electrode: relatively large and placed between stimulating and recording electrodes

SNAP characteristics

- Conduction velocity Can be determined with one stimulation site (ascompared with the motor conduction velocity thatrequires two stimulation sites)

- Compound potential that is summation of individual nerve action potentials, may be biphasic or triphasic.

- Usually more sensitive to both generalized and focalnerve disease than motor nerve conduction studies (e.g., entrapment mononeuropathies such as carpal tunnel syndrome)

- SNAP abnormalities may be first abnormalities of a neuropathic process such as generalized sensorimotor neuropathy (earlier than motor studies) and may be selectively involved in sensory neuropathies.

- Proximal sensory studies result in smaller amplitudepotentials and are difficult to perform

Note: Onset latency is not affected by temporal dispersion and phase cancellation and can be used to measure conduction velocity.

Why SNAPs potentially may be abnormal in lower lumbar or upper sacral radiculopathies

Because the DRG of lower lumbar and upper sacral segments may be inside the spinal canal and axonal injury related to a compressive radiculopathy in these segments may be at or distal to the DRG, SNAPs potentially may be abnormal in lower lumbar or upper sacral radiculopathies

b. Conduction velocity and distal latency may be normal, assuming largest and fastest conducting axons are intact (Large reduction of amplitude and some slowing of conduction velocity or mild prolongation of distal latencies may indicate axonal loss, with relative loss of large fast-conducting fibers and relative preservation of slowlyconducting fibers) --> Conduction velocities may be decreased, but neverless than 70% of lower limit of normal and Distal latencies expected to be normal or slightly prolonged,but no more than 130% of upper limit of normal.

C. With hyperacute lesions, nerve conduction studies performedwithin first 4 to 6 days may be normal

Demyelination (motor and sensory conduction studies)

a. Slowing of conduction velocities: slower than 70% of lower limit of normal if amplitudes are preserved, 50% if amplitudes are decreased

b. Prolongation of distal latency, Longer than 130% of upper limit of normal

c. Focal slowing --> More than 10 m/s slowing over 10-cm segment and More than 0.4-millisecond change in latency over1-cm segment

d. Temporal dispersion and phase cancellation

f. complete block --> loss of CMAP

Inherited demyelinating polyneuropathies

Usually all myelin is affected equally and demyelination is symmetric --> Slowing is uniform --> Dispersion and block are uncommon

Normal late responses (F waves and H waves)

F waves:

- Named “F” because originally recorded from the foot

- Both afferent and efferent arms are motor; no synapse involved

- Not a true reflex

- May be spared in conditions selectively involving sensorypathways or a relatively small number of motor axons

- Produced by impulse traveling antidromically (like F waves) to a branch point in the nerve and then orthodromically along the second branch (unlike F waves )toward the recording electrode to create an A-wave response

- May be seen in peripheral neuropathy, polyradiculopathy, or plexopathy

- Usually do not occur in normal subjects

- Initial antidromic impulse: latency decreases when stimulation site is moved proximally (as with F waves)

Posttetanic potentiation or facilitation vs. Decrement

In summary: potentiation oraugmentation of the amount of acetylcholine released after brief repetitive exercise or rapid rate of stimulation (>10 Hz)

But

Decrement: reduction in amount of acetylcholine released with slow rates of repetitive stimulation (2-3Hz), caused by depletion of acetylcholine stores in activezones of nerve terminal

note : Normally, safety margin of neuromuscular transmissionis large, and no decrement of CMAP occursdespite the decrease in EPP amplitude (see the pic)

b) Repetitive stimulation at slow rates may cause lower subsequent EPPs that may not reach the threshold, causing transmission failure across neuromuscular junction and CMAP decrement

c) CMAP decrement is greatest between first and second stimuli in a train of four stimuli

d) Immediately after exercise, there is postactivation facilitation of CMAP amplitude and decrease inthe decremental response

e) There is a greater decremental response 4 minutesafter exercise

Repetitive nerve stimulation: Normal vs. MG

Note: Brief period of exercise has same effect as rapid stimulation at 20 to 50 Hz, and is more tolerable.

a. In normal subjects --> no decrement should occur with 2-Hz stimulation and Immediately after exercise, normal subjects may show small increments in responses caused by synchronizedfiring of motor units.

b. In MG --> Decrement with repetitive stimulation at 2 Hz --> Greatest relative change between the first and second response in the train of four stimuli.

and Repair of decrement with exercise or rapid stimulation at 20 to 50 Hz

Larger decrement noted 1 to 3 minutes after exerciseg.

Repetitive nerve stimulation: Lambert-Eaton myasthenic syndrome

1) Low-amplitude resting CMAP

2) Decrement with repetitive stimulation at 2 Hz,usually less prominent than in myasthenia gravis

Rapid recruitment: recruitment of many MUPs (near interference pattern, with minimal muscle contraction, always associated with reduction in size of MUPs) --> Usually seen in myopathies due to loss of individual muscle fiber

Poor activation signifies poor voluntary effort or a central lesion

Insertional Activity

Increased insertional activity

a. Normal variants

b. Neuropathic conditions

c. Myopathic conditions

Reduced insertional activity: seen in long-standing neuropathic or myopathic conditions in which muscle is replaced by connective tissue

Fibrillation potentials

Seen in denervation as well as myopathic or severe NM junction blocking.

A-D, Fibrillation potentials of different amplitudes and severity. Smaller amplitudes may occur with advanced muscleatrophy. Note regular firing of each waveform. Note also fasciculation potential at beginning of recording in C. This was recordedfrom anterior tibialis muscle in patient with amyotrophic lateral sclerosis.

Are fibrillation potentials and positive sharp waves the same?

No! Although in most cases these two potentials have the same clinical significance, there are at least five different situations in which they do not have an identical meaning:

(1) positive sharp waves can be recorded earlier after a peripheral nerve injury than can fibrillation potentials;

Myotonic discharge recorded from patient with myotonic dystrophy. In addition, there were slow, tall fibrillation potentials (arrows) in the recording, two of which are shown here. The myotonic discharge ends with the second fibrillation potential represented in this segment.

Neuromyotonic discharges

High-frequency (100-300 Hz) regular repetitive discharges of a single MUP characteristically wanes in amplitude and frequency

c. By 4 weeks, MUPs will likely have increased duration and be polyphasic.

e. Reinnervation eventually produces long-duration, high amplitude neurogenic potentials, which may become less polyphasic over time in absence of ongoing denervation

f. By this stage, amplitudes of CMAPs (if preganglionic or postganglionic localization of lesion) and SNAPs (if postganglionic) may be reduced, with relative preservation of conduction velocities and distal latencies

a. Nerve conduction studies are expected to be normal or show reduced amplitude, depending on severity of axonal injury and success of reinnervation (conduction velocities may be mildly reduced because re innervated axons have smaller diameter and less myelin)

b. “Nascent units” may be present with proximal-to-distal reinnervation

c. Both collateral and proximal-to-distal reinnervation eventually result in long-duration, high-amplitude, stable MUPs with reduced recruitment, which may or may not be polyphasic.

d. Insertional activity is often normal, in absence of ongoing denervation

Nascent units

True axonal regeneration leads to the formation of nascent potentials, which are usually low in amplitude, polyphasic in configuration, and can have a short or normal and sometimes even long duration.

Terminal collateral sprouting always leads to the formation of long-duration polyphasics. Although both are polyphasic, their configuration is distinctly different and it is important to remember that only the nascent potentials represent true axonal regeneration.

“Nascent units.” Early nascent units have shortduration and low amplitude, but with ongoing reinnervationthey become more polyphasic and duration increases, as seenhere. Note the severely reduced recruitment that distinguishesthese potentials from myopathic motor unit potentials. Also,there is variability of motor unit potentials due to neuromuscularjunction instability.

b. Chronic severe or end-stage myopathies may appear “neurogenic” (i.e., long duration, large amplitude, polyphasic), probably because of excessive motor unit remodeling that occurs with advanced disease of the muscle fibers.